Shock Overview

Patrcia M. Veiga C. Mello, M.D.,1,2

M.D.,3
4
and R. Phillip Dellinger, M.D.

Vinay K. Sharma,

ABSTRACT

Despite improved understanding of the pathophysiology of shock and significant

advances in technology, it remains a serious problem associated with high morbidity and
mortality. Early treatment is essential but is hampered by the fact that signs and
symptoms of shock appear only after the shock state is well established and the bodys
compensatory mechanisms have started to fail. Although the causes of shock are
varied, the basic abnormality in all varieties is tissue and cellular dysoxia. In this
overview we discuss the definition, classification and pathogenesis of shock in light of
the recent advances in our understanding of its mechanisms. The epidemiology,
diagnosis, and management of the various types of shock are also briefly discussed.
KEYWORDS: Shock, hypoperfusion, septic shock, cardiogenic shock, hypovolemic

shock

Objectives: Upon completion of this article, the reader will: (1) appreciate divergent pathophysiology of different causes of shock; (2)
understand the importance of intervention on systemic manifestations of shock; and (3) be familiar with an algorithmic approach to
resuscitation of shock patients.
Accreditation: The University of Michigan is accredited by the Accreditation Council for Continuing Medical Education to sponsor
continuing medical education for physicians.
Credits: The University of Michigan designates this educational activity for a maximum of 1 category 1 credit toward the AMA
Physicians Recognition Award.

hock is likely the most serious diagnosis made

in intensive care units worldwide. Its etiology is varied
and complex and optimal resuscitation and intervention
varies with etiology. Aggressive diagnostic and therapeutic interventions must occur simultaneously to avoid
irreversible cellular injury and microcirculatory failure.
Shock remains a major cause of mortality in any setting
in which it appears and without the appropriate diagnostic and therapeutic approach it is almost invariably
lethal. Despite significant technological advances in
critical care medicine, the combination of delay in

diagnosis and incomplete understanding of its intricate

pathophysiology results in high mortality rates. Optimal
management requires a multidisciplinary team, ideally
1,2
led by an intensivist, in a hospital setting with appropriate diagnostic and management capabilities.
HISTORICAL ASPECTS
Hippocrates described a posttraumatic syndrome
long before shock syndrome was used as a medical term.
The word shock is derived from the French word choquer,

Management of Shock; Editor in Chief, Joseph P. Lynch, III, M.D.; Guest Editors, Arthur P. Wheeler, M.D., Gordon R. Bernard, M.D. Seminars
in Respiratory and Critical Care Medicine, volume 25, number 6, 2004. Address for correspondence and reprint requests: R. Phillip Dellinger, M.D.,
Critical Care Section, Cooper University Hospital, One Cooper Plaza, 393 Dorrance, Camden, NJ 08103. E-mail: dellinger-phil@cooperhealth.
1
2
edu. Department of Critical Care Medicine, Hospital Sao Marcos, Teresina, Piau, Brazil; Hospital de Terapia Intensiva, Faculdade de
3
Ciencias Medicas, Universidade Estadual do Piau, Teresina, Piau, Brazil; Pulmonary and Critical Care Medicine Division, Graduate
4
Hospital, Drexel University, Philadelphia, Pennsylvania; Critical Care Section, Cooper University Hospital, Camden, New Jersey. Copyright #
2004 by Thieme Medical Publishers, Inc., 333 Seventh Avenue, New York, NY 10001, USA. Tel: +1(212) 584-4662. 10693424,p;2004,25,06,619,628,ftx,en; srm00335x.

619

108

SEMINARS IN RESPIRATORY AND CRITICAL CARE MEDICINE/VOLUME 25, NUMBER 6

meaning to collide with. The term choc was first used

by a French surgeon, Le Dran, to indicate a severe
3
impact or jolt, but it was not until 1867 that the term
became popularized when Edwin Morris published his
4
Practical Treatise on Shock after Operations and Injuries.
He defined it as a peculiar effect on the animal system,
produced by violent injuries from any cause, or from
violent mental emotions calling attention to a bodys
response to injury for the first time as opposed to
focusing on the immediate manifestations of trauma
itself. By the late 1800s, Fisher suggested that a
general- ized vasomotor paralysis resulting in
5
splanchnic blood pooling was the cause of shock, and
a few years later Maphoter, suggested extravascular
leakage of fluids was the cause of the clinical
6
findings seen in traumatic shock.
In the 1900s Cannon, based on his battlefield
experience during World War I, attributed the initiation
of shock to more than mere blood loss with a
disturbance of the nervous system causing relaxation of
7
blood vessels and hypotension. He proposed that a
toxic factor was released during shock leading to altered
capillary perme- ability and loss of blood volume from
the intravascular space. In 1930, Alfred Blalock
challenged Cannons theory, arguing that blood loss
8
would sufficiently explain the fall in cardiac output. In
the 1940s a cardiovascular physiologist, Carl Wiggers,
published a series of studies demonstrating that a
prolonged shock state could lead to irreversible
9
circulatory failure. Fluid resuscitation be- came the
standard of care in the management of these patients.
Hypotension had become not only the hallmark of shock
but also the endpoint followed by most physi- cians
while managing these patients.
For a long time shock was considered to occur
only as a result of trauma. It was not until
1898,
during the Spanish American War, that sepsis was
10
described to cause shock.
In
1906 Rosenau
published his obser- vations of a severe reaction
occurring after a second injection of some foreign
proteins (i.e., anaphylactic shock). In 1935 Tennant
and Wiggers demonstrated an immediate drop in
myocardial contraction when the heart was acutely
11
deprived of coronary perfusion.

Table 1

2004

DEFINITION
The definition of shock has continued to change considerably over the years. It can no longer be based on
blood pressure alone. Assessment of perfusion independent of arterial pressure has clearly demonstrated that
adequate blood pressure does not equal adequate
12,13
cardiac output or tissue perfusion.
Seemingly
adequate oxy- gen delivery (DO2) also does not
guarantee oxygen or substrate utilization at a cellular
level. In sepsis, there is evidence suggesting that a
cellular disturbance may impair oxygen and substrate
14,15
utilization.
Cyanide or carbon monoxide
intoxication leads to cellular cytotoxic hypoxia, despite
the presence of adequate DO2. Situa- tions as may
occur with sepsis and cyanide or carbon monoxide
poisoning have led to the concept of cyto- toxic or
cytopathic shock. In light of these new con- cepts,
regardless of the mechanism by which it occurs, when
cellular dysoxia occurs, a shock state is present, which
ultimately leads to organ dysfunction and failure.
CLASSIFICATION
Shock has traditionally been classified into four categories: hypovolemic, distributive, cardiogenic, and obstructive shock. More appropriate is to classify shock
into five categories to include cytotoxic shock (Table 1).
EPIDEMIOLOGY AND ETIOLOGY
The incidence and prevalence of shock are currently
unknown. Several factors make it difficult to perform
epidemiological analysis of this entity. Regardless of its
etiology, patients may die before getting to the hospital.
Furthermore, it is not a reportable diagnosis and there
is still a lack of consensus regarding the definition of
shock in general, and specific forms of shock. Not
surprisingly there is great variability in reported shock
incidence and mortality rates. Despite all these
epidemiological diffi- culties, it is well known that all
types of shock carry a very high mortality.
Cardiogenic shock is the number one cause of
mortality from coronary artery disease in the United

Classification of Shock and Its Most Common Etiologies

Hypovolemic
Cardiogenic

Obstructive
Distributive
Cytotoxic

External and occult hemorrhages, skin losses (severe burns), third-spacing (pancreatitis, bowel obstruction, and
prolonged abdominal surgery), gastrointestinal tract losses (vomiting, diarrhea), urinary tract losses
Acute myocardial infarction and its complications (e.g., acute mitral regurgitation, rupture of the interventricular
septum, rupture of the free wall), myocarditis, end-stage cardiomyopathy, myocardial contusion, myocardial
dysfunction after prolonged cardiopulmonary bypass, valvular heart disease, and hypertrophic obstructive
cardiomyopathy
Cardiac tamponade, massive pulmonary embolism, tension pneumothorax, cor pulmonale, atrial myxoma,
coarctation of aorta
Septic shock, anaphylactic shock, neurogenic shock, adrenal crisis
Cyanide intoxication, carbon monoxide intoxication, iron intoxication

16

States. Estimated incidence ranges between 6 and

8%,1720 and this rate has remained fairly stable from
21
1975 to 1997. In the largest registry of patients with
cardiogenic shock, 75% of patients had predominant left
ventricular failure, 8% had acute mitral regurgitation,
5% had ventricular septal rupture, 3% had isolated
right
ventricular shock, 2% had tamponade or cardiac rupture,
and 8% had shock resulting from other causes (such as
myocarditis, end-stage cardiomyopathy, myocardial contusion, myocardial dysfunction after prolonged cardiopulmonary bypass, valvular heart disease, and
22
hypertrophic obstructive cardiomyopathy). Early reperfusion strategies have improved survival rates in
21
recent studies but mortality remains high.
Several
studies have reported lower rates of shock (47%) with
20,2325
the use of thrombolytics in myocardial infarction,
although no evidence has been found that this therapy is
17,25
beneficial once shock has occurred.
Even lower
mortality rates are reported with revascularization stra26,27
tegies.
Despite advanced supportive care in the
management of heart failure and acute myocardial infarction, cardiogenic shock is still the most common
cause of in-hospital mortality in transmural myocardial
infarction, with overall mortality rates remaining be22,18
tween 70 and 90%.
Accurate assessment of the incidence of septic
shock is also difficult to ascertain. In a study by the
Centers for Disease Control and Prevention, the inci28
dence of sepsis in 1989 was 176 per 100,000. Septic
shock is reported as the thirteenth most frequent cause
29
of mortality in the United States.
A recent metaanalysis found the mortality rate from septic shock to
30
be > 40% in most studies analyzed. The mortality
rate from septic shock observed in the placebo arms of
randomized controlled trials have decreased over time
most probably due to advances in supportive care
(Table 2). Once the predominant cause of sepsis, gramnegative bacteria now account for
38% of cases,
31
whereas 52% are due to gram-positive bacteria.
There has also been a dramatic (207%) increase in
31
fungi as a cause of sepsis.
Hypovolemic shock remains a major cause of
death in trauma patients but may also be seen as a
complication of surgery and in patients with burns and
gastrointestinal bleeding. Trauma patients may also
have
Table 2 Change in Septic Shock Mortality Rates
over Time
Period

No. of
Studies

No. of
Patients

Hospital Mortality
Rate (%)

19581969*
19701979*
19801989*
19901997*
19971992

13
17
39
62
30

668
1378
2594
6256
7874

61
53
55
45
39

*Adapted from Friedman et al.

30

obstructive or neurogenic shock. Regardless of comorbidities or injuries, the shock state by itself will greatly
affect these patients prognosis and will be responsible
32,33
for significant increases in morbidity and mortality.
PATHOPHYSIOLOGY
Cardiogenic shock occurs when myocardial damage
(acute or acute on chronic) reaches a point where
pump function is markedly impaired. As one enters
cardiogenic shock, stroke volume and cardiac output
decrease, reducing myocardial perfusion, which, in
turn, exacerbates ischemia and creates a downward
spiral. Compensatory mechanisms that are activated by
decreasing myocardial function eventually become maladaptive. Increased heart rate and increased afterload
resulting from catecholamine release increase
myocardial oxygen demand and worsen ischemia.
Impaired diastolic filling due to tachycardia and
ischemia, combined with the kidneys attempt to
increase preload by retaining fluid, result in pulmonary
congestion and hypoxia.
Obstructive shock is characterized by inadequate
ventricular filling due to cardiac compression or severe
obstruction to ventricular inflow or outflow. In cardiac
tamponade inadequate heart filling leads to decreased
cardiac output, decreased blood pressure, reflex vasoconstriction, and elevated intracardiac pressures despite
inadequate filling. Massive pulmonary embolism leads
to obstruction of the pulmonary vessels by clot and
release of vasoconstrictive mediators. Elevation of
right-sided pressures with a normal pulmonary artery
occlusion pressure and low cardiac output reflects right
ventricular failure due to increased pulmonary
resistance.
Hypovolemic shock is characterized by loss of
circulating volume. Hypovolemia, tissue injury, and
pain result in an increase in sympathetic drive in an
attempt to raise blood pressure by increasing heart rate,
cardiac contractility, and peripheral vasomotor tone.
Although initially beneficial, these adaptive measures
can eventually be harmful because the hypermetabolic
state induced by the sympathetic drive can make tissues
more susceptible to local ischemia. Uneven peripheral
vasoconstriction can result in maldistributive microcirculatory flow and tissue hypoxia. Compensatory
mechanisms fail when volume loss is > 25%. An
impor- tant inflammatory component also occurs in
severe
34,35
hypovolemic shock.
Delays of just 2 hours in appropriate resuscitation from volume losses exceeding 40%
may result in inability to effectively correct tissue hypo36
perfusion. Despite adequate control of volume loss, the
patient may die as a consequence of the systemic activation of the inflammatory cascade triggered by the initial
insult that can be further aggravated by reperfusion
37,38
injury phenomenon.
The characteristic feature of distributive shock is
a decline in peripheral vascular resistance. Septic shock

is

the classic example, but several other conditions can lead

to a similar hemodynamic profile. Trauma to the spinal
cord may lead to neurogenic shock that is characterized
by an autonomic dysfunction with loss of peripheral
vascular tone with a relative hypovolemic state and
severe hypotension. Bradycardia may also be present
and further impair cardiac output. In anaphylactic
shock, severe immunoglobulin E (IgE)-mediated
immediate hypersensitivity leads to massive release of
mediators from mast cells and basophiles (especially
histamine) resulting in decreased vascular resistance,
capillary leak, and impaired contractility. Adrenal crisis
is another form of distributive shock, which, when
volume resuscitated, evokes a hemodynamic profile
similar to septic shock.
Tumor necrosis factor alpha (TNF-a) and interleukin-1 (IL-1) are the dominant cytokines in septic
39
shock. Increased TNF-a levels are also seen in heart
40
34
failure and hemorrhagic shock. TNF-a is produced
by macrophages in response to microbial antigens and
other cytokines. It results in the release of additional
inflammatory mediators (IL-1b, IL-6, IL-8, thromboxanes, platelet-activating factor, and eicosanoids), which
activate the coagulation and complement systems, depress myocardial contractility, and lead to vasodilation
41,42
through inducible nitric oxide synthase activation.
Nitric oxide is a key player in distributive shock
where it serves multiple physiological roles, including
neurotransmission, regulation of tissue perfusion via
vascular
tone
and
responsiveness,
platelet
responsiveness, renal
volume control,
and
43,44
antimicrobial defense.
Nitric oxide is the major mediator of vasodilation and
45,46
hypotension in septic shock
and may also be in47
volved in the development of myocardial depression. It
has also been implicated in vascular dysfunction seen in
35
hemorrhagic shock.
Oxygen Metabolism
In general, constant oxygen consumption (VO2) is
maintained over a wide range of DO2. At some critical
point, oxygen extraction cannot increase any further, and
reductions in DO2 will result in a reduction in VO2
(Fig. 1). This physiological oxygen supply dependency is
primarily seen during low output circulatory shock. It
was initially thought that a pathological oxygen supply
dependency was present in patients with septic shock
(i.e., the critical DO2 point is increased and VO2 is
dependent on DO2 over a wider range); however, this
4850
relationship is unlikely.
In shock, decreased perfusion leads to limited
oxidative metabolism resulting in lactic acidosis from
anaerobic metabolism. The degree of lactate elevation
correlates with both the degree of hypoperfusion and the
51
mortality rate. Regional hypoperfusion is indicated by
52,53
decreased gastric intramucosal pH
and hepatic ve54
nous oxygen desaturation. However, in most patients

Figure 1 Relationship between oxygen consumption (VO2) and

oxygen delivery (DO2).

with septic shock, there also appears to be an inability

15
of the tissues to extract oxygen from the blood.
Thus lactic acidosis may occur despite normal cardiac
output and mixed venous oxygen saturation (SvO2). In
cardio- genic and hypovolemic shock, lactic acidosis
occurs only after severe reduction in SvO2.
DIAGNOSIS
The first step for successful outcome with a shock state
is early recognition. It is important to keep in mind
that diabetic, cirrhotic, neutropenic, and elderly patients
may develop septic shock without a typical clinical
picture or obvious source of
infection.
Basic
evaluation should include metabolic panel, hemogram,
arterial blood gas, electrocardiogram, and chest x-ray.
It is important to remember that a drop in hemoglobin
level occurs late in hemorrhagic shock and volume loss
is best assessed by signs of hypoperfusion. The
echocardiogram is increas- ingly being used in the
assessment of patients in shock; it is noninvasive, can
be performed at bedside, and can immediately reveal
or exclude several potential etiologies of the shock state.
Recent studies have suggested that procalcitonin level is
a good marker of infection and may help differentiate
55,56
septic from other shock states.
Initial physical examination should focus on identifying signs of tissue hypoperfusion and on
differentiat- ing cardiogenic shock from other types of
shock because initial volume resuscitation may be
different in the former. If signs of fluid overload are
absent, a possible source of volume loss or infection
should be aggressively sought. No sign, symptom, or
laboratory test by itself is diagnostic of shock, perhaps
with the exception of profound hypotension. Shock is
easy to diagnose when a patient arrives in the
emergency department with multiple stab wounds,
profuse bleeding, and immeasur- able blood pressure.
The
problem is recognizing it in more subtle
presentations. It is necessary to maintain a high index
of suspicion and be alert to a group of nonspecific
signs and symptoms that in the appropriate clinical
context permits an early diagnosis of shock.

Table 3

Hemodynamic Profiles and Main Therapeutic Intervention in the Various Shock States

Hemodynamic Profiles
of Shock
Hypovolemic
Cardiogenic
Septic
Prior to fluids
After fluids
Pulmonary Embolism
Pericardial tamponade
Anaphylactic
Prior to fluids
After fluids
Adrenal
Prior to fluids
After fluids

Cardiac Output

Preload

Afterload

Contractility

Intervention

#
#

#
"

"
"

N
#

Crystalloid or colloid, blood

Inotropes, vasopressors
Fluids, vasopressors

# to N
"
#
#

#
N
#
#

#
#
"
"

#
#
N
N

to N
"

#
N

#
#

#
#

to N

"

Thrombolytic therapy
Pericardiocentesis
Fluids, inotropes, vasopressors

Fluids, steroids, inotropes, vasopressors

Hypotension is present in most shock states and

will usually catch the attention of the physician, but
unfortunately only occurs once the compensatory mechanisms are overwhelmed. In hypovolemic shock, tachycardia occurs after 15% of the circulating volume is
lost. However, despite being a sensitive sign of shock it
is nonspecific, and it is important to be aware that
this response may be blunted in patients who are on
b- blockers or calcium channel blockers. Mottled skin
and cold extremities, altered consciousness, thirst,
concen- trated urine, oliguria, and elevated creatinine
may be present. In hemorrhage almost 30% of
volume will be
57
lost before the patient becomes hypotensive. An earlier
sign is narrowing of the pulse pressure due to catecholamine-stimulated elevation of diastolic blood pressure
57
in response to the low circulating volume. Furthermore, not only can shock occur in the absence of
hypotension, it may persist even once hypotension has
been reversed. Blood pressure may be maintained with
vasopressors at the cost of worsening oxygen debt.
Measurement of lactic acid is a useful tool to
assess severity and follow adequacy of therapeutic man58,59
euvers,
but lactic acid changes may not occur early
enough to be a sentinel marker for shock. At least in
sepsis, elevated lactic acid levels have been shown to
60
occur with normal intracellular oxygenation. Furthermore, elevated lactic acid levels may occur due to
comorbid conditions, especially liver failure because it
is cleared by the liver. However, in a recent post hoc
analysis of early, goal-directed therapy in septic patients
with lactic acidosis (> 4 mmol/L) and mean arterial
pressure above 100 mm Hg, patients in the protocol
group had significantly lower mortality than those in the
61
standard therapy group.
Measurement of cardiac output and SvO2, as well
as calculation of DO2, VO2, and oxygen extraction
ratios can be achieved with a pulmonary artery (PA)
catheter. Despite the controversies regarding its
62,63
use,
the

catheter is widely used, and much of its reported

negative effect on outcome may be the result of
poor under- standing and improper utilization of
64
data.
In addition to ascertaining filling pressures,
flow, and oxygen in- dices, specific pathological
diagnoses linked to shock may be made (Table 3).
Elevated right-sided and low PA occlusion pressure in
the setting of acute inferior myo- cardial infarction
should raise the suspicion of right ventricular
65
infarct. Central venous oxygen saturation (ScvO2) is
easier to obtain than pulmonary artery mixed venous
saturation and may potentially be a good surro- gate
66
for SvO2 in septic shock.
Hypoperfusion is the hallmark of shock. Assessment of oxygen transport parameters is the best way of
determining
the
presence of
global
tissue
hypoperfusion. However, regional tissue hypoperfusion
may be present despite normal values of oxygen
transport variables, base deficit, and lactic acid levels.
Gastric tonometry has been shown to predict mortality
and may help determine splanchnic perfusion and
67,68
guide resuscitation.
How- ever, the difficulty of
technique and interpretation of the data, and the
increased cost associated with gastric tonometry,
have limited its clinical applicability.
Cardiogenic shock may present with signs of
increased central venous pressure, pulmonary edema,
third heart sound, and peripheral vasoconstriction;
although pulmonary edema may be absent in right
ventricular infarct. Arrhythmia and mitral regurgitation
murmur may also be present. Echocardiography helps
evaluate systolic function and can reveal papillary muscle
rupture, mitral regurgitation, ventricular septal defects,
69
and free-wall rupture.
Kussmauls sign, pulsus paradoxus, distant heart
sounds on auscultation, and decreased voltage on electrocardiogram may be present in cardiac tamponade.
Equalization of pressures is diagnostic of this condition
with mean right atrial, right ventricular end diastolic,
and PA occlusion pressures within 5 mm Hg of one

another. The central venous pressure tracing may show a

rapid x descent and a blunted y descent, reflecting
ventricular inflow obstruction. Echocardiogram reveals
pericardial effusion, and may show ventricular septal
deviation to the left and right ventricular collapse during
systole.
Distributive shock, frequently referred as warm
shock, is characterized by peripheral vasodilation and a
hyperdynamic cardiac status that prevails until later
stages when myocardial depression ultimately leads to
decreased cardiac output. Evidence of infection,
presence of spinal trauma or a trigger for anaphylaxis
will help

Figure 2

Diagnostic and management approach to shock.

differentiate the underlying etiology. Adrenal crisis may

present with abdominal pain, nausea, vomiting, hypothermia, refractory hypotension, hyponatremia, and
hyperkalemia.
MANAGEMENT
The approach to the patient with shock must be
dynamic with diagnostic and therapeutic maneuvers
occurring simultaneously, striving to avoid further
injury, by improving tissue perfusion (Fig. 2). With the
exception of cardiogenic shock, aggressive fluid
resuscitation is

usually required. However, cardiogenic shock due to

right ventricular infarction also requires volume resuscitation. Fluids should be given until signs of hypoperfusion resolve or signs of volume overload appear.
Constant reassessment is key and the effects of each
therapeutic intervention on signs of tissue hypoperfusion
should guide therapy. There has been no conclusive
evidence favoring the use of either crystalloid or colloid
70
solutions in volume resuscitation. Blood transfusion
should be instituted to maintain an adequate DO2
57
and/or SvO2 or when significant blood loss is apparent.
Endotracheal intubation and mechanical ventilation are
often required.
Adequate assessment of intravascular volume status is a challenge. Occult hypovolemia due to extravascular loss of fluid is frequently underestimated and
peripheral edema is often mistakenly used as a sign of
intravascular volume overload. Studies have shown that
71,72
neither physical examination
nor central venous
73,74
pressure monitoring
is accurate in determining left
ventricular volume status. For that purpose a PA catheter
placement offers a more accurate assessment of intravascular volume status and tissue perfusion, better delineation of the hemodynamic profile, and dynamic
observation of the effect of each therapeutic intervention
(Table 3). It can help guide both fluid resuscitation and
vasopressor or positive inotrope titration. However, use
of a PA catheter is controversial given recent studies
indicating no benefit or perhaps even harm from placement. The PA catheter has some limitations; cardiac
output measured by thermodilution may be falsely increased (e.g., in severe tricuspid regurgitation or in
intracardiac shunt). In such instances, cardiac output
calculation using Ficks method may be used in addition
to the PA catheter to more accurately estimate cardiac
output and tissue perfusion. Noninvasive methods of
estimating cardiac output include thoracic electrical
75
76
bioimpedance and pulse contour analysis. However,
77
the accuracy of these systems has been questioned.
In cardiogenic shock, therapeutic measures include early revascularization strategies, emergency surgery, intraaortic balloon pump, and artificial ventricular
support devices (LVAD [left ventricular assist device] /
BiVAD [biventricular assist device]). Revascularization
strategies have proven to be most beneficial if under27,78,79
taken within the first few hours after the insult.
Obstructive shock due to cardiac tamponade requires needle, catheter, or surgical drainage of the
pericardial fluid. Fluid and vasoactive drugs may be
required to support circulation while awaiting decompression. In shock due to pulmonary embolism, cardiac
arrhythmias should be corrected, a fluid challenge given,
and thrombolytic therapy considered. The role of vasoactive drugs is less clear.
In hypovolemic shock, volume resuscitation is
indicated and vasopressors should be avoided if
possible,

though often administered during initial resuscitation.

Several studies performed in the trauma population have
shown worse outcome with aggressive volume resuscitation prior to bleeding control, probably due to disruption
8082
of the hemostatic plug.
However, delayed resuscitation may exacerbate the inflammatory component triggered by hypovolemic shock leading to multiple organ
37,83
failure and death.
Therefore, it seems that judicious
fluid resuscitation to maintain hemodynamic stability
with avoidance of overload prior to bleeding control is
prudent.
In septic shock, the initial treatment remains
antibiotic therapy and source control. Appropriate anti84,85
biotic therapy improves outcome.
In addition, volume resuscitation is paramount. The fluid deficit in
septic shock is often 6 L or more in the first 24 hours
and vasopressor support should not be utilized in
place of adequate intravascular volume. Traditionally,
86
dopamine has been the vasopressor of choice.
However, one study has suggested that norepinephrine
is more easily titrated to achieve hemodynamic goals
87
and may be associated with better outcome. A recent
study has emphasized the importance of instituting
aggressive therapy early and targeting normal ScvO2
88
saturation. Recombinant human activated protein C
has been clearly demon- strated to improve outcome
89
in septic shock.
In septic shock patients with
impaired adrenal responsiveness, hydrocortisone plus
90
fluorocortisone may also improve survival.
It has been suggested that maintaining a supranormal cardiac output in patients with shock should
increase DO2 and VO2, decrease any oxygen debt present, and potentially improve survival. Randomized
controlled trials have been performed to test this
strategy but found that supranormal cardiac output and
DO2 did not lower mortality when used to reverse
9196
tissue hypoxia (as in septic patients).
However,
when used in a prophylactic approach (i.e., before
organ failure devel- ops), there appears to be a survival
97101
advantage.
When shock occurs due to more than one etiology, a mixture of signs may be present and the hemodynamic profile will not show the classic pattern of one
particular type of shock, but a mixture of features. It is
important to be able to recognize such a patient and
adapt the management accordingly. The physical signs
and hemodynamic profiles may also be altered by preexisting comorbidities. Cirrhotic and pregnant patients
have a lower systemic vascular resistance and a hyperdynamic hemodynamic profile in the absence of a distributive shock. Pregnant patients have a higher
circulating volume that may mask early signs of
shock. Athletes have a higher circulating volume and
cardiac output, and a lower resting heart rate. Thus
signs of shock may also be delayed in these patients.
Patients with heart block and a pacemaker may not be
able to mount a tachycardic response.

CONCLUSIONS
Shock continues to result in substantial morbidity and
mortality despite significant advances in technology and
pathophysiological understanding. Initial priority is
aimed at the general principles of resuscitation: assuring
adequate airway and oxygenation, vascular access, and
volume resuscitation. The goal of therapy is to restore
adequate tissue perfusion. Manipulation of the blood
oxygen content and cardiac ouput may improve tissue
perfusion. Early diagnosis, aggressive resuscitation, and
interruption or reversal of the insult (i.e., control of
bleeding, myocardial revascularization strategies, infection control) is the optimal approach in managing the
patient in shock.
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3. LeDran HF. A Treatise, or Reflections Drawn from Practice
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Showing translation for EPIDEMIOLOGY AND

ETIOLOGY The incidence and prevalence of shock are
currently unknown. Several factors make it difficult to
perform epidemiological analysis of this entity.
Regardless of its etiology, patients may die before
getting to the hospital. Furthermore, it is not a
reportable diagnosis and there is still a lack of
consensus regarding the definition of shock in general,
and specific forms of shock. Not surprisingly there is
great variability in reported shock incidence and
mortality rates. Despite all these epidemiological
difficulties, it is well known that all types of shock
carry a very high mortality. Cardiogenic shock is the
number one cause of mortality from coronary artery
disease in the United Table 1 Classification of Shock
and Its Most Common Etiologies Hypovolemic
External and occult hemorrhages, skin losses (severe
burns), third-spacing (pancreatitis, bowel obstruction,
and prolonged abdominal surgery), gastrointestinal
tract losses (vomiting, diarrhea), urinary tract losses
Cardiogenic Acute myocardial infarction and its
complications (e.g., acute mitral regurgitation, rupture
of the interventricular septum, rupture of the free wall),
myocarditis, end-stage cardiomyopathy, myocardial
contusion, myocardial dysfunction after prolonged
cardiopulmonary bypass, valvular heart disease, and
hypertrophic obstructive cardiomyopathy Obstructive
Cardiac tamponade, massive pulmonary embolism,
tension pneumothorax, cor pulmonale, atrial myxoma,
coarctation of aorta Distributive Septic shock,
anaphylactic shock, neurogenic shock, adrenal crisis
Cytotoxic Cyanide intoxication, carbon monoxide
intoxication, iron intoxication States.16 Estimated
incidence ranges between 6 and 8%,1720 and this rate
has remained fairly stable from 1975 to 1997.21 In the
largest registry of patients with cardiogenic shock, 75%
of patients had predominant left ventricular failure, 8%
had acute mitral regurgitation, 5% had ventricular
septal rupture, 3% had isolated right ventricular shock,
2% had tamponade or cardiac rupture, and 8% had
shock resulting from other causes (such as myocarditis,
end-stage cardiomyopathy, myocardial con- tusion,
myocardial dysfunction after prolonged cardiopulmonary bypass, valvular heart disease, and
hypertrophic obstructive cardiomyopathy).22 Early re-

perfusion strategies have improved survival

rates in recent studies but mortality remains
high.21 Several studies have reported lower
rates of shock (47%) with the use of
thrombolytics in myocardial infarction,20,23
25 although no evidence has been found that
this therapy is beneficial once shock has
occurred.17,25 Even lower mortality rates are
reported with revascularization strategies.26,27 Despite advanced supportive care
in the management of heart failure and acute
myocardial in- farction, cardiogenic shock is
still the most common cause of in-hospital
mortality in transmural myocardial infarction,
with overall mortality rates remaining be- tween
70 and 90%.22,18 Accurate assessment of the
incidence of septic shock is also difficult to
ascertain. In a study by the Centers for Disease
Control and Prevention, the inci- dence of
sepsis in 1989 was 176 per 100,000.28 Septic
shock is reported as the thirteenth most frequent
cause of mortality in the United States.29 A
recent meta-analysis found the mortality rate
from septic shock to be > 40% in most studies
analyzed.30 The mortality rate from septic
shock observed in the placebo arms of
randomized controlled trials have decreased
over time most probably due to advances in
supportive care (Table 2). Once the
predominant cause of sepsis, gram-negative
bacteria now account for 38% of cases, whereas
52% are due to gram-positive bacteria.31 There
has also been a dramatic (207%) increase in
fungi as a cause of sepsis.31 Hypovolemic
shock remains a major cause of death in trauma
patients but may also be seen as a complication
of surgery and in patients with burns and
gastrointestinal bleeding. Trauma patients may
also have Table 2 Change in Septic Shock
Mortality Rates over Time obstructive or
neurogenic shock. Regardless of comor- bidities
or injuries, the shock state by itself will greatly
affect these patients prognosis and will be
responsible for significant increases in
morbidity and mortality.32,33
PATHOPHYSIOLOGY Cardiogenic shock
occurs when myocardial damage (acute or acute
on chronic) reaches a point where pump
function is markedly impaired. As one enters
cardiogenic shock, stroke volume and cardiac
output decrease, reducing myocardial perfusion,
which, in turn, exacerbates ischemia and creates

a downward spiral. Compensatory mechanisms that are

activated by decreasing myocardial function eventually
become ma- ladaptive. Increased heart rate and
increased afterload resulting from catecholamine
release increase myocardial oxygen demand and
worsen ischemia. Impaired diastolic filling due to
tachycardia and ischemia, combined with the kidneys
attempt to increase preload by retaining fluid, result in
pulmonary congestion and hypoxia. Obstructive shock
is characterized by inadequate ventricular filling due to
cardiac compression or severe obstruction to
ventricular inflow or outflow. In cardiac tamponade
inadequate heart filling leads to decreased cardiac
output, decreased blood pressure, reflex vasoconstriction, and elevated intracardiac pressures despite
inadequate filling. Massive pulmonary embolism leads
to obstruction of the pulmonary vessels by clot and
release of vasoconstrictive mediators. Elevation of
right-sided pressures with a normal pulmonary artery
occlusion pressure and low cardiac output reflects right
ventricular failure due to increased pulmonary
resistance. Hypovolemic shock is characterized by loss
of circulating volume. Hypovolemia, tissue injury, and
pain result in an increase in sympathetic drive in an
attempt to raise blood pressure by increasing heart rate,
cardiac contractility, and peripheral vasomotor tone.
Although initially beneficial, these adaptive measures
can eventually be harmful because the hypermetabolic
state induced by the sympathetic drive can make tissues
more susceptible to local ischemia. Uneven peripheral
vasoconstriction can result in maldistributive microcirculatory flow and tissue hypoxia. Compensatory
mechanisms fail when volume loss is > 25%. An
impor- tant inflammatory component also occurs in
severe hypovolemic shock.34,35 Delays of just 2 hours
in appro- priate resuscitation from volume losses
exceeding 40% No. of No. of Hospital Mortality may
result in inability to effectively correct tissue hypoPeriod Studies Patients Rate (%) 19581969* 13 668
61 19701979* 17 1378 53 19801989* 39 2594 55
19901997* 62 6256 45 19971992 30 7874 39
*Adapted from Friedman et al.30 perfusion.36 Despite
adequate control of volume loss, the patient may die as
a consequence of the systemic activa- tion of the
inflammatory cascade triggered by the initial insult that
can be further aggravated by reperfusion injury
phenomenon.37,38 The characteristic feature of
distributive shock is a decline in peripheral vascular
resistance. Septic shock is the classic example, but
several other conditions can lead to a similar
hemodynamic profile. Trauma to the spinal cord may
lead to neurogenic shock that is characterized by an

autonomic dysfunction with loss of peripheral

vascular tone with a relative hypovolemic state
and severe hypotension. Bradycardia may also
be present and further impair cardiac output. In
anaphylactic shock, severe immunoglobulin E
(IgE)-mediated immediate hypersensitivity
leads to massive release of mediators from mast
cells and basophiles (especially histamine)
resulting in decreased vascular resistance,
capillary leak, and impaired contractility.
Adrenal crisis is another form of distributive
shock, which, when volume resuscitated,
evokes a hemodynamic profile similar to septic
shock. Tumor necrosis factor alpha (TNF-a) and
inter- leukin-1 (IL-1) are the dominant
cytokines in septic shock.39 Increased TNF-a
levels are also seen in heart failure40 and
hemorrhagic shock.34 TNF-a is produced by
macrophages in response to microbial antigens
and other cytokines. It results in the release of
additional inflammatory mediators (IL-1b, IL-6,
IL-8, thrombox- anes, platelet-activating factor,
and eicosanoids), which activate the
coagulation and complement systems, de- press
myocardial contractility, and lead to
vasodilation through inducible nitric oxide
synthase activation.41,42 Nitric oxide is a key
player in distributive shock where it serves
multiple physiological roles, including
neurotransmission, regulation of tissue
perfusion via vascular tone and responsiveness,
platelet responsiveness, renal volume control,
and antimicrobial defense.43,44 Nitric oxide is
the major mediator of vasodilation and
hypotension in septic shock45,46 and may also
be in- volved in the development of myocardial
depression.47 It has also been implicated in
vascular dysfunction seen in hemorrhagic
shock.35 Oxygen Metabolism In general,
constant oxygen consumption (VO2) is
maintained over a wide range of DO2. At some
critical point, oxygen extraction cannot increase
any further, and reductions in DO2 will result in
a reduction in VO2 (Fig. 1). This physiological
oxygen supply dependency is primarily seen
during low output circulatory shock. It was
initially thought that a pathological oxygen
supply dependency was present in patients with
septic shock (i.e., the critical DO2 point is
increased and VO2 is dependent on DO2 over a
wider range); however, this relationship is
unlikely.4850 In shock, decreased perfusion

leads to limited oxidative metabolism resulting in lactic

acidosis from anaerobic metabolism. The degree of
lactate elevation correlates with both the degree of
hypoperfusion and the mortality rate.51 Regional
hypoperfusion is indicated by decreased gastric
intramucosal pH52,53 and hepatic ve- nous oxygen
desaturation.54 However, in most patients Figure 1
Relationship between oxygen consumption (VO2) and
oxygen delivery (DO2). with septic shock, there also
appears to be an inability of the tissues to extract
oxygen from the blood.15 Thus lactic acidosis may
occur despite normal cardiac output and mixed venous
oxygen saturation (SvO2). In cardio- genic and
hypovolemic shock, lactic acidosis occurs only after
severe reduction in SvO2. DIAGNOSIS The first step
for successful outcome with a shock state is early
recognition. It is important to keep in mind that
diabetic, cirrhotic, neutropenic, and elderly patients
may develop septic shock without a typical clinical
picture or obvious source of infection. Basic evaluation
should include metabolic panel, hemogram, arterial
blood gas, electrocardiogram, and chest x-ray. It is
important to remember that a drop in hemoglobin level
occurs late in hemorrhagic shock and volume loss is
best assessed by signs of hypoperfusion. The
echocardiogram is increas- ingly being used in the
assessment of patients in shock; it is noninvasive, can
be performed at bedside, and can immediately reveal or
exclude several potential etiologies of the shock state.
Recent studies have suggested that procalcitonin level
is a good marker of infection and may help differentiate
septic from other shock states.55,56 Initial physical
examination should focus on iden- tifying signs of
tissue hypoperfusion and on differentiat- ing
cardiogenic shock from other types of shock because
initial volume resuscitation may be different in the
former. If signs of fluid overload are absent, a possible
source of volume loss or infection should be
aggressively sought. No sign, symptom, or laboratory
test by itself is diagnostic of shock, perhaps with the
exception of profound hypotension. Shock is easy to
diagnose when a patient arrives in the emergency
department with multiple stab wounds, profuse
bleeding, and immeasur- able blood pressure. The
problem is recognizing it in more subtle presentations.
It is necessary to maintain a high index of suspicion
and be alert to a group of nonspecific signs and
symptoms that in the appropriate clinical context
permits an early diagnosis of shock. Table 3
Hemodynamic Profiles and Main Therapeutic
Intervention in the Various Shock States Hemodynamic
Profiles of Shock Cardiac Output Preload Afterload

Contractility Intervention Hypovolemic # # " N

Crystalloid or colloid, blood Cardiogenic Septic
# " " # Inotropes, vasopressors Fluids,
vasopressors Prior to fluids After fluids
Pulmonary Embolism # to N " # # N # # # " # #
N Thrombolytic therapy Pericardial tamponade
Anaphylactic # # " N Pericardiocentesis Fluids,
inotropes, vasopressors Prior to fluids After
fluids Adrenal to N " # N # # # # Fluids,
steroids, inotropes, vasopressors Prior to fluids
to N # # N After fluids " N # N Hypotension is
present in most shock states and will usually
catch the attention of the physician, but
unfortunately only occurs once the
compensatory me- chanisms are overwhelmed.
In hypovolemic shock, ta- chycardia occurs
after 15% of the circulating volume is lost.
However, despite being a sensitive sign of
shock it is nonspecific, and it is important to be
aware that this response may be blunted in
patients who are on b- blockers or calcium
channel blockers. Mottled skin and cold
extremities, altered consciousness, thirst,
concen- trated urine, oliguria, and elevated
creatinine may be present. In hemorrhage
almost 30% of volume will be lost before the
patient becomes hypotensive.57 An earlier sign
is narrowing of the pulse pressure due to
catecho- lamine-stimulated elevation of
diastolic blood pressure in response to the low
circulating volume.57 Further- more, not only
can shock occur in the absence of hypotension,
it may persist even once hypotension has been
reversed. Blood pressure may be maintained
with vasopressors at the cost of worsening
oxygen debt. Measurement of lactic acid is a
useful tool to assess severity and follow
adequacy of therapeutic man- euvers,58,59 but
lactic acid changes may not occur early enough
to be a sentinel marker for shock. At least in
sepsis, elevated lactic acid levels have been
shown to occur with normal intracellular
oxygenation.60 Further- more, elevated lactic
acid levels may occur due to comorbid
conditions, especially liver failure because it is
cleared by the liver. However, in a recent post
hoc analysis of early, goal-directed therapy in
septic patients with lactic acidosis (> 4 mmol/L)
and mean arterial pressure above 100 mm Hg,
patients in the protocol group had significantly
lower mortality than those in the standard
therapy group.61 Measurement of cardiac

output and SvO2, as well as calculation of DO2, VO2,

and oxygen extraction ratios can be achieved with a
pulmonary artery (PA) catheter. Despite the
controversies regarding its use,62,63 the catheter is
widely used, and much of its reported negative effect
on outcome may be the result of poor under- standing
and improper utilization of data.64 In addition to
ascertaining filling pressures, flow, and oxygen indices, specific pathological diagnoses linked to shock
may be made (Table 3). Elevated right-sided and low
PA occlusion pressure in the setting of acute inferior
myo- cardial infarction should raise the suspicion of
right ventricular infarct.65 Central venous oxygen
saturation (ScvO2) is easier to obtain than pulmonary
artery mixed venous saturation and may potentially be
a good surro- gate for SvO2 in septic shock.66
Hypoperfusion is the hallmark of shock. Assess- ment
of oxygen transport parameters is the best way of
determining the presence of global tissue
hypoperfusion. However, regional tissue hypoperfusion
may be present despite normal values of oxygen
transport variables, base deficit, and lactic acid levels.
Gastric tonometry has been shown to predict mortality
and may help determine splanchnic perfusion and
guide resuscitation.67,68 How- ever, the difficulty of
technique and interpretation of the data, and the
increased cost associated with gastric tonometry, have
limited its clinical applicability. Cardiogenic shock may
present with signs of increased central venous pressure,
pulmonary edema, third heart sound, and peripheral
vasoconstriction; although pulmonary edema may be
absent in right ventricular infarct. Arrhythmia and
mitral regurgitation murmur may also be present.
Echocardiography helps evaluate systolic function and
can reveal papillary muscle rupture, mitral
regurgitation, ventricular septal defects, and free-wall
rupture.69 Kussmauls sign, pulsus paradoxus, distant
heart sounds on auscultation, and decreased voltage on
elec- trocardiogram may be present in cardiac
tamponade. Equalization of pressures is diagnostic of
this condition with mean right atrial, right ventricular
end diastolic, and PA occlusion pressures within 5 mm
Hg of one another. The central venous pressure tracing
may show a rapid x descent and a blunted y
descent, reflecting ventricular inflow obstruction.
Echocardiogram reveals pericardial effusion, and may
show ventricular septal deviation to the left and right
ventricular collapse during systole. Distributive shock,
frequently referred as warm shock, is characterized
by peripheral vasodilation and a hyperdynamic cardiac
status that prevails until later stages when myocardial
depression ultimately leads to decreased cardiac output.

Evidence of infection, presence of spinal trauma

or a trigger for anaphylaxis will help
differentiate the underlying etiology. Adrenal
crisis may present with abdominal pain, nausea,
vomiting, hy- pothermia, refractory
hypotension, hyponatremia, and hyperkalemia.
Translate instead EPIDEMIOLOGY AND
ETIOLOGY The incidence and prevalence of
shock are currently unknown. Several factors
make it difficult to perform epidemiological
analysis of this entity. Regardless of its etiology,
patients may die before getting to the hospital.
Furthermore, it is not a reportable diagnosis and
there is still a lack of consensus regarding the
definition of shock in general, and specific
forms of shock. Not surprisingly there is great
variability in reported shock incidence and
mortality rates. Despite all these
epidemiological diffi- culties, it is well known
that all types of shock carry a very high
mortality. Cardiogenic shock is the number one
cause of mortality from coronary artery disease
in the United Table 1 Classification of Shock
and Its Most Common Etiologies Hypovolemic
External and occult hemorrhages, skin losses
(severe burns), third-spacing (pancreatitis,
bowel obstruction, and prolonged abdominal
surgery), gastrointestinal tract losses (vomiting,
diarrhea), urinary tract losses Cardiogenic
Acute myocardial infarction and its
complications (e.g., acute mitral regurgitation,
rupture of the interventricular septum, rupture
of the free wall), myocarditis, end-stage
cardiomyopathy, myocardial contusion,
myocardial dysfunction after prolonged
cardiopulmonary bypass, valvular heart disease,
and hypertrophic obstructive cardiomyopathy
Obstructive Cardiac tamponade, massive
pulmonary embolism, tension pneumothorax,
cor pulmonale, atrial myxoma, coarctation of
aorta Distributive Septic shock, anaphylactic
shock, neurogenic shock, adrenal crisis
Cytotoxic Cyanide intoxication, carbon
monoxide intoxication, iron intoxication
States.16 Estimated incidence ranges between 6
and 8%,1720 and this rate has remained fairly
stable from 1975 to 1997.21 In the largest
registry of patients with cardiogenic shock, 75%
of patients had predominant left ventricular
failure, 8% had acute mitral regurgitation, 5%
had ventricular septal rupture, 3% had isolated
right ventricular shock, 2% had tamponade or

cardiac rupture, and 8% had shock resulting from other

causes (such as myocarditis, end-stage cardiomyopathy,
myocardial con- tusion, myocardial dysfunction after
prolonged cardio- pulmonary bypass, valvular heart
disease, and hypertrophic obstructive
cardiomyopathy).22 Early re- perfusion strategies have
improved survival rates in recent studies but mortality
remains high.21 Several studies have reported lower
rates of shock (47%) with the use of thrombolytics in
myocardial infarction,20,2325 although no evidence
has been found that this therapy is beneficial once
shock has occurred.17,25 Even lower mortality rates
are reported with revascularization stra- tegies.26,27
Despite advanced supportive care in the management
of heart failure and acute myocardial in- farction,
cardiogenic shock is still the most common cause of inhospital mortality in transmural myocardial infarction,
with overall mortality rates remaining be- tween 70 and
90%.22,18 Accurate assessment of the incidence of
septic shock is also difficult to ascertain. In a study by
the Centers for Disease Control and Prevention, the
inci- dence of sepsis in 1989 was 176 per 100,000.28
Septic shock is reported as the thirteenth most frequent
cause of mortality in the United States.29 A recent
meta-analysis found the mortality rate from septic
shock to be > 40% in most studies analyzed.30 The
mortality rate from septic shock observed in the
placebo arms of randomized controlled trials have
decreased over time most probably due to advances in
supportive care (Table 2). Once the predominant cause
of sepsis, gram-negative bacteria now account for 38%
of cases, whereas 52% are due to gram-positive
bacteria.31 There has also been a dramatic (207%)
increase in fungi as a cause of sepsis.31 Hypovolemic
shock remains a major cause of death in trauma
patients but may also be seen as a complication of
surgery and in patients with burns and gastrointestinal
bleeding. Trauma patients may also have Table 2
Change in Septic Shock Mortality Rates over Time
obstructive or neurogenic shock. Regardless of comorbidities or injuries, the shock state by itself will greatly
affect these patients prognosis and will be responsible
for significant increases in morbidity and
mortality.32,33 PATHOPHYSIOLOGY Cardiogenic
shock occurs when myocardial damage (acute or acute
on chronic) reaches a point where pump function is
markedly impaired. As one enters cardiogenic shock,
stroke volume and cardiac output decrease, reducing
myocardial perfusion, which, in turn, exacerbates
ischemia and creates a downward spiral. Compensatory
mechanisms that are activated by decreasing
myocardial function eventually become ma- ladaptive.

Increased heart rate and increased afterload

resulting from catecholamine release increase
myocardial oxygen demand and worsen
ischemia. Impaired diastolic filling due to
tachycardia and ischemia, combined with the
kidneys attempt to increase preload by
retaining fluid, result in pulmonary congestion
and hypoxia. Obstructive shock is characterized
by inadequate ventricular filling due to cardiac
compression or severe obstruction to ventricular
inflow or outflow. In cardiac tamponade
inadequate heart filling leads to decreased
cardiac output, decreased blood pressure, reflex
vasocon- striction, and elevated intracardiac
pressures despite inadequate filling. Massive
pulmonary embolism leads to obstruction of the
pulmonary vessels by clot and release of
vasoconstrictive mediators. Elevation of rightsided pressures with a normal pulmonary artery
occlusion pressure and low cardiac output
reflects right ventricular failure due to increased
pulmonary resistance. Hypovolemic shock is
characterized by loss of circulating volume.
Hypovolemia, tissue injury, and pain result in
an increase in sympathetic drive in an attempt
to raise blood pressure by increasing heart rate,
cardiac contractility, and peripheral vasomotor
tone. Although initially beneficial, these
adaptive measures can eventually be harmful
because the hypermetabolic state induced by the
sympathetic drive can make tissues more
susceptible to local ischemia. Uneven
peripheral vasoconstriction can result in
maldistributive microcir- culatory flow and
tissue hypoxia. Compensatory mechanisms fail
when volume loss is > 25%. An impor- tant
inflammatory component also occurs in severe
hypovolemic shock.34,35 Delays of just 2 hours
in appro- priate resuscitation from volume
losses exceeding 40% No. of No. of Hospital
Mortality may result in inability to effectively
correct tissue hypo- Period Studies Patients
Rate (%) 19581969* 13 668 61 19701979*
17 1378 53 19801989* 39 2594 55 1990
1997* 62 6256 45 19971992 30 7874 39
*Adapted from Friedman et al.30 perfusion.36
Despite adequate control of volume loss, the
patient may die as a consequence of the
systemic activa- tion of the inflammatory
cascade triggered by the initial insult that can be
further aggravated by reperfusion injury
phenomenon.37,38 The characteristic feature of

distributive shock is a decline in peripheral vascular

resistance. Septic shock is the classic example, but
several other conditions can lead to a similar
hemodynamic profile. Trauma to the spinal cord may
lead to neurogenic shock that is characterized by an
autonomic dysfunction with loss of peripheral vascular
tone with a relative hypovolemic state and severe
hypotension. Bradycardia may also be present and
further impair cardiac output. In anaphylactic shock,
severe immunoglobulin E (IgE)-mediated immediate
hypersensitivity leads to massive release of mediators
from mast cells and basophiles (especially histamine)
resulting in decreased vascular resistance, capillary
leak, and impaired contractility. Adrenal crisis is
another form of distributive shock, which, when
volume resuscitated, evokes a hemodynamic profile
similar to septic shock. Tumor necrosis factor alpha
(TNF-a) and inter- leukin-1 (IL-1) are the dominant
cytokines in septic shock.39 Increased TNF-a levels are
also seen in heart failure40 and hemorrhagic shock.34
TNF-a is produced by macrophages in response to
microbial antigens and other cytokines. It results in the
release of additional inflammatory mediators (IL-1b,
IL-6, IL-8, thrombox- anes, platelet-activating factor,
and eicosanoids), which activate the coagulation and
complement systems, de- press myocardial
contractility, and lead to vasodilation through inducible
nitric oxide synthase activation.41,42 Nitric oxide is a
key player in distributive shock where it serves
multiple physiological roles, including
neurotransmission, regulation of tissue perfusion via
vascular tone and responsiveness, platelet
responsiveness, renal volume control, and
antimicrobial defense.43,44 Nitric oxide is the major
mediator of vasodilation and hypotension in septic
shock45,46 and may also be in- volved in the
development of myocardial depression.47 It has also
been implicated in vascular dysfunction seen in
hemorrhagic shock.35 Oxygen Metabolism In general,
constant oxygen consumption (VO2) is maintained
over a wide range of DO2. At some critical point,
oxygen extraction cannot increase any further, and
reductions in DO2 will result in a reduction in VO2
(Fig. 1). This physiological oxygen supply dependency
is primarily seen during low output circulatory shock.
It was initially thought that a pathological oxygen
supply dependency was present in patients with septic
shock (i.e., the critical DO2 point is increased and VO2
is dependent on DO2 over a wider range); however,
this relationship is unlikely.4850 In shock, decreased
perfusion leads to limited oxidative metabolism
resulting in lactic acidosis from anaerobic metabolism.

The degree of lactate elevation correlates with

both the degree of hypoperfusion and the
mortality rate.51 Regional hypoperfusion is
indicated by decreased gastric intramucosal
pH52,53 and hepatic ve- nous oxygen
desaturation.54 However, in most patients
Figure 1 Relationship between oxygen
consumption (VO2) and oxygen delivery
(DO2). with septic shock, there also appears to
be an inability of the tissues to extract oxygen
from the blood.15 Thus lactic acidosis may
occur despite normal cardiac output and mixed
venous oxygen saturation (SvO2). In cardiogenic and hypovolemic shock, lactic acidosis
occurs only after severe reduction in SvO2.
DIAGNOSIS The first step for successful
outcome with a shock state is early recognition.
It is important to keep in mind that diabetic,
cirrhotic, neutropenic, and elderly patients may
develop septic shock without a typical clinical
picture or obvious source of infection. Basic
evaluation should include metabolic panel,
hemogram, arterial blood gas,
electrocardiogram, and chest x-ray. It is
important to remember that a drop in
hemoglobin level occurs late in hemorrhagic
shock and volume loss is best assessed by signs
of hypoperfusion. The echocardiogram is
increas- ingly being used in the assessment of
patients in shock; it is noninvasive, can be
performed at bedside, and can immediately
reveal or exclude several potential etiologies of
the shock state. Recent studies have suggested
that procalcitonin level is a good marker of
infection and may help differentiate septic from
other shock states.55,56 Initial physical
examination should focus on iden- tifying signs
of tissue hypoperfusion and on differentiat- ing
cardiogenic shock from other types of shock
because initial volume resuscitation may be
different in the former. If signs of fluid overload
are absent, a possible source of volume loss or
infection should be aggressively sought. No
sign, symptom, or laboratory test by itself is
diagnostic of shock, perhaps with the exception
of profound hypotension. Shock is easy to
diagnose when a patient arrives in the
emergency department with multiple stab
wounds, profuse bleeding, and immeasur- able
blood pressure. The problem is recognizing it in
more subtle presentations. It is necessary to
maintain a high index of suspicion and be alert

to a group of nonspecific signs and symptoms that in

the appropriate clinical context permits an early
diagnosis of shock. Table 3 Hemodynamic Profiles and
Main Therapeutic Intervention in the Various Shock
States Hemodynamic Profiles of Shock Cardiac Output
Preload Afterload Contractility Intervention
Hypovolemic # # " N Crystalloid or colloid, blood
Cardiogenic Septic # " " # Inotropes, vasopressors
Fluids, vasopressors Prior to fluids After fluids
Pulmonary Embolism # to N " # # N # # # " # # N
Thrombolytic therapy Pericardial tamponade
Anaphylactic # # " N Pericardiocentesis Fluids,
inotropes, vasopressors Prior to fluids After fluids
Adrenal to N " # N # # # # Fluids, steroids, inotropes,
vasopressors Prior to fluids to N # # N After fluids " N
# N Hypotension is present in most shock states and
will usually catch the attention of the physician, but
unfortunately only occurs once the compensatory mechanisms are overwhelmed. In hypovolemic shock, tachycardia occurs after 15% of the circulating volume is
lost. However, despite being a sensitive sign of shock it
is nonspecific, and it is important to be aware that this
response may be blunted in patients who are on bblockers or calcium channel blockers. Mottled skin and
cold extremities, altered consciousness, thirst, concentrated urine, oliguria, and elevated creatinine may be
present. In hemorrhage almost 30% of volume will be
lost before the patient becomes hypotensive.57 An
earlier sign is narrowing of the pulse pressure due to
catecho- lamine-stimulated elevation of diastolic blood
pressure in response to the low circulating volume.57
Further- more, not only can shock occur in the absence
of hypotension, it may persist even once hypotension
has been reversed. Blood pressure may be maintained
with vasopressors at the cost of worsening oxygen
debt. Measurement of lactic acid is a useful tool to
assess severity and follow adequacy of therapeutic
man- euvers,58,59 but lactic acid changes may not
occur early enough to be a sentinel marker for shock.
At least in sepsis, elevated lactic acid levels have been
shown to occur with normal intracellular
oxygenation.60 Further- more, elevated lactic acid
levels may occur due to comorbid conditions,
especially liver failure because it is cleared by the liver.
However, in a recent post hoc analysis of early, goaldirected therapy in septic patients with lactic acidosis
(> 4 mmol/L) and mean arterial pressure above 100
mm Hg, patients in the protocol group had significantly
lower mortality than those in the standard therapy
group.61 Measurement of cardiac output and SvO2, as
well as calculation of DO2, VO2, and oxygen
extraction ratios can be achieved with a pulmonary

artery (PA) catheter. Despite the controversies

regarding its use,62,63 the catheter is widely
used, and much of its reported negative effect
on outcome may be the result of poor understanding and improper utilization of data.64 In
addition to ascertaining filling pressures, flow,
and oxygen in- dices, specific pathological
diagnoses linked to shock may be made (Table
3). Elevated right-sided and low PA occlusion
pressure in the setting of acute inferior myocardial infarction should raise the suspicion of
right ventricular infarct.65 Central venous
oxygen saturation (ScvO2) is easier to obtain
than pulmonary artery mixed venous saturation
and may potentially be a good surro- gate for
SvO2 in septic shock.66 Hypoperfusion is the
hallmark of shock. Assess- ment of oxygen
transport parameters is the best way of
determining the presence of global tissue
hypoperfusion. However, regional tissue
hypoperfusion may be present despite normal
values of oxygen transport variables, base
deficit, and lactic acid levels. Gastric tonometry
has been shown to predict mortality and may
help determine splanchnic perfusion and guide
resuscitation.67,68 How- ever, the difficulty of
technique and interpretation of the data, and the
increased cost associated with gastric
tonometry, have limited its clinical applicability.
Cardiogenic shock may present with signs of
increased central venous pressure, pulmonary
edema, third heart sound, and peripheral
vasoconstriction; although pulmonary edema
may be absent in right ventricular infarct.
Arrhythmia and mitral regurgitation murmur
may also be present. Echocardiography helps
evaluate systolic function and can reveal
papillary muscle rupture, mitral regurgitation,
ventricular septal defects, and free-wall
rupture.69 Kussmauls sign, pulsus paradoxus,
distant heart sounds on auscultation, and
decreased voltage on elec- trocardiogram may
be present in cardiac tamponade. Equalization
of pressures is diagnostic of this condition with
mean right atrial, right ventricular end diastolic,
and PA occlusion pressures within 5 mm Hg of
one another. The central venous pressure tracing
may show a rapid x descent and a blunted
y descent, reflecting ventricular inflow
obstruction. Echocardiogram reveals pericardial
effusion, and may show ventricular septal
deviation to the left and right ventricular

collapse during systole. Distributive shock, frequently

referred as warm shock, is characterized by
peripheral vasodilation and a hyperdynamic cardiac
status that prevails until later stages when myocardial
depression ultimately leads to decreased cardiac output.
Evidence of infection, presence of spinal trauma or a
trigger for anaphylaxis will help differentiate the
underlying etiology. Adrenal crisis may present with
abdominal pain, nausea, vomiting, hy- pothermia,
refractory hypotension, hyponatremia, and
hyperkalemia.
EPIDEMIOLOGI DAN ETIOLOGI
Insiden dan prevalensi syok saat ini tidak diketahui.
Beberapa faktor membuat sulit untuk melakukan
analisis epidemiologi dari entitas ini. Terlepas dari
etiologinya, pasien mungkin meninggal sebelum
sampai ke rumah sakit. Selain itu, bukan diagnosis
dilaporkan dan masih ada kurangnya konsensus
mengenai definisi syok pada umumnya, dan bentukbentuk khusus dari shock. Tidak mengherankan ada
variabilitas yang besar dalam melaporkan kejadian
shock dan mortalitas. Meskipun semua kesulitan
epidemiologi ini, adalah juga diketahui bahwa semua
jenis shock membawa kematian sangat tinggi.
syok kardiogenik adalah nomor satu penyebab
kematian dari penyakit arteri koroner di Inggris
Tabel 1 Klasifikasi Syok dan Its Etiologi Paling Umum
Hipovolemik Eksternal dan perdarahan okultisme,
kerugian kulit (luka bakar), ketiga spasi (pankreatitis,
obstruksi usus, dan pembedahan perut
berkepanjangan), kerugian saluran pencernaan
(muntah, diare), kerugian saluran kemih
infark miokard akut kardiogenik dan komplikasinya
(misalnya, regurgitasi akut mitral, pecahnya septum
interventrikular, pecahnya dinding gratis), miokarditis,
stadium akhir kardiomiopati, memar miokard,
disfungsi miokard setelah memotong berkepanjangan
cardiopulmonary, penyakit jantung katup, dan
hipertrofi kardiomiopati obstruktif
Obstruktif tamponade jantung, emboli paru masif,
ketegangan pneumotoraks, cor pulmonale, myxoma
atrium, koarktasio aorta
syok distributif Septic, shock anafilaksis, shock
neurogenik, krisis adrenal
Sitotoksik Sianida keracunan, keracunan karbon
monoksida, keracunan besi
Insiden Perkiraan States.16 berkisar antara 6 dan
8%, 17-20 dan tingkat ini tetap cukup stabil dari
1975-1997,21 Dalam registry terbesar pasien dengan
syok kardiogenik, 75% pasien memiliki kegagalan
ventrikel kiri yang dominan, 8% memiliki regurgitasi
mitral akut, 5% memiliki ruptur septum ventrikel, 3%

memiliki hak terisolasi

syok ventrikel, 2% memiliki tamponade atau
ruptur jantung, dan 8% memiliki kejutan yang
dihasilkan dari penyebab lain (seperti
miokarditis, stadium akhir kardiomiopati, tusion
con- miokard, disfungsi miokard setelah
memotong paru cardio berkepanjangan,
penyakit jantung katup, dan hipertrofi
kardiomiopati obstruktif) .22 strategi perfusi reawal telah meningkat tingkat ketahanan hidup
di studi terbaru tapi kematian tetap Beberapa
penelitian high.21 telah melaporkan tingkat
yang lebih rendah shock (4-7%) dengan
menggunakan trombolitik di infark miokard,
20,23- 25 meskipun tidak ada bukti telah
ditemukan bahwa terapi ini sangat bermanfaat
sekali kejutan memiliki occurred.17,25 Bahkan
lebih rendah tingkat kematian dilaporkan
dengan tegies.26,27 revaskularisasi strameskipun perawatan suportif maju dalam
pengelolaan gagal jantung dan di- miokard akut
farction, syok kardiogenik masih merupakan
penyebab paling umum kematian di rumah sakit
di infark miokard transmural, dengan tingkat
kematian secara keseluruhan sisa tween 70 dan
90% .22,18
penilaian yang akurat dari kejadian syok septik
juga sulit dipastikan. Dalam sebuah studi oleh
Pusat Pengendalian dan Pencegahan Penyakit,
yang insidensi sepsis pada tahun 1989 adalah
176 per 100,000.28 syok septik dilaporkan
sebagai penyebab paling sering ketiga belas dari
kematian di States.29 Inggris A meta-analisis ini
ditemukan mortalitas tingkat dari syok septik
menjadi> 40% di kebanyakan studi analyzed.30
tingkat kematian dari syok septik diamati di
lengan plasebo dari uji coba terkontrol secara
acak telah menurun dari waktu ke waktu yang
paling mungkin karena kemajuan dalam
perawatan suportif (Tabel 2). Setelah penyebab
dominan dari sepsis, bakteri gram negatif
sekarang account untuk 38% dari kasus,
sedangkan 52% adalah karena gram-positif
bacteria.31 Ada juga dramatis (207%)
peningkatan jamur sebagai penyebab sepsis. 31
syok hipovolemik tetap menjadi penyebab
utama kematian pada pasien trauma, tetapi juga
dapat dilihat sebagai komplikasi dari operasi
dan pada pasien dengan luka bakar dan
perdarahan gastrointestinal. pasien trauma
mungkin juga memiliki
Tabel 2 Perubahan Septic shock Angka

Kematian lebih Waktu

obstruktif atau neurogenic shock. Terlepas dari bidities
comor- atau cedera, negara kejutan dengan sendirinya
akan sangat mempengaruhi prognosis pasien ini 'dan
akan bertanggung jawab untuk peningkatan yang
signifikan dalam morbiditas dan mortality.32,33
PATOFISIOLOGI
syok kardiogenik terjadi ketika kerusakan miokard
(akut atau akut pada kronis) mencapai titik di mana
fungsi pompa nyata terganggu. Sebagai salah satu
memasuki syok kardiogenik, stroke volume dan
penurunan curah jantung, mengurangi perfusi miokard,
yang, pada gilirannya, memperburuk iskemia dan
menciptakan spiral. mekanisme kompensasi yang
diaktifkan oleh penurunan fungsi miokard akhirnya
menjadi ladaptive ma-. Peningkatan denyut jantung dan
peningkatan afterload akibat katekolamin rilis
peningkatan kebutuhan oksigen miokard dan
memperburuk iskemia. pengisian diastolik gangguan
karena takikardia dan iskemia, dikombinasikan dengan
upaya ginjal untuk meningkatkan preload dengan
mempertahankan cairan, mengakibatkan kemacetan
paru dan hipoksia.
syok obstruktif ditandai dengan pengisian ventrikel
yang tidak memadai karena kompresi jantung atau
obstruksi parah inflow ventrikel atau keluar. Dalam
tamponade jantung mengisi jantung yang tidak
memadai menyebabkan penurunan curah jantung,
tekanan darah menurun, vasokonstriksi refleks, dan
tekanan intrakardiak tinggi meskipun mengisi
memadai. emboli paru masif menyebabkan obstruksi
pembuluh paru oleh bekuan dan pelepasan mediator
vasokonstriksi. Peningkatan tekanan sisi kanan dengan
normal paru tekanan oklusi arteri dan curah jantung
yang rendah mencerminkan kegagalan ventrikel kanan
karena peningkatan resistensi paru.
syok hipovolemik ditandai dengan hilangnya volume
sirkulasi. Hipovolemia, cedera jaringan, dan hasilnya
rasa sakit peningkatan dalam drive simpatik dalam
upaya untuk meningkatkan tekanan darah dengan
meningkatkan denyut jantung, kontraktilitas jantung,
dan tonus vasomotor perifer. Meski awalnya
menguntungkan, langkah-langkah adaptif akhirnya
dapat berbahaya karena keadaan hipermetabolik yang
disebabkan oleh drive simpatik dapat membuat
jaringan lebih rentan terhadap iskemia lokal. Merata
vasokonstriksi perifer dapat mengakibatkan
maldistributive aliran culatory microcir- dan hipoksia
jaringan. mekanisme kompensasi gagal ketika
kehilangan volume> 25%. Komponen inflamasi tant
impor- juga terjadi di parah
Penundaan shock.34,35 hipovolemik hanya 2 jam di

tindakanresusitasi priate dari kerugian volume yang

melebihi 40%
Jumlah
Jumlah
Kematian rumah sakit
dapat mengakibatkan ketidakmampuan untuk
secara efektif benar jaringan hipo Studi Periode
Pasien Rate (%)
1958-1969 * 13 668 61
1970-1979 * 17 1378 53
1980-1989 * 39 2594 55
1990-1997 * 62 6256 45 1997-1992 30 7874 39
* Diadaptasi dari Friedman et al.30
perfusion.36 Meskipun kontrol yang memadai
dari hilangnya volume, pasien mungkin mati
sebagai konsekuensi dari aktifasi sistemik dari
kaskade inflamasi dipicu oleh penghinaan awal
yang dapat lebih diperburuk oleh cedera
reperfusi phenomenon.37,38
Fitur karakteristik syok distributif adalah
penurunan resistensi pembuluh darah perifer.
syok septik adalah
contoh klasik, namun beberapa kondisi lain
dapat menyebabkan profil yang sama
hemodinamik. Trauma pada sumsum tulang
belakang dapat menyebabkan syok neurogenik
yang ditandai dengan disfungsi otonom dengan
hilangnya tonus pembuluh darah perifer dengan
keadaan dan berat hipovolemik hipotensi relatif.
Bradikardia juga dapat hadir dan selanjutnya
merusak cardiac output. Pada syok anafilaktik,
berat imunoglobulin E (IgE) -dimediasi segera
hipersensitivitas mengarah ke rilis besar
mediator dari sel mast dan basophiles (terutama
histamin) yang mengakibatkan resistensi
menurun vaskular, kebocoran kapiler, dan
gangguan kontraktilitas. Krisis adrenal adalah
bentuk lain dari syok distributif, yang, ketika
volume diresusitasi, membangkitkan profil
hemodinamik mirip dengan syok septik.
Tumor necrosis factor alpha (TNF-a) dan antar
interleukin-1 (IL-1) adalah sitokin yang
dominan di shock.39 septic Peningkatan TNF-a
tingkat juga terlihat di failure40 jantung dan
hemorrhagic shock.34 TNF-a diproduksi oleh
makrofag dalam menanggapi antigen mikroba
dan sitokin lainnya. Hasilnya pelepasan
mediator tambahan inflamasi (IL-1b, IL-6, IL-8,
anes thrombox-, platelet-activating factor, dan
eikosanoid), yang mengaktifkan koagulasi dan
melengkapi sistem, de- tekan kontraktilitas

miokard, dan menyebabkan vasodilatasi melalui

diinduksi nitrat oksida sintase activation.41,42
Nitrat oksida adalah pemain kunci dalam syok
distributif mana melayani peran ganda fisiologis,
termasuk neurotransmisi, regulasi perfusi jaringan
melalui tonus pembuluh darah dan responsif, tanggap
platelet, kontrol volume ginjal, dan defense.43,44
antimikroba
Nitrat oksida adalah mediator utama vasodilatasi dan
hipotensi di shock45,46 septik dan mungkin juga
dilibatkan dalam pengembangan depression.47
miokard Ini juga telah terlibat dalam disfungsi vaskular
dilihat di hemoragik shock.35
oksigen metabolisme
Secara umum, konsumsi oksigen yang konstan (VO2)
dipertahankan selama berbagai DO2. Di beberapa titik
kritis, ekstraksi oksigen tidak dapat meningkatkan lebih
jauh, dan pengurangan DO2 akan menghasilkan
pengurangan VO2 (Gambar. 1). suplai oksigen
ketergantungan fisiologis ini terutama terlihat selama
output yang rendah kejutan peredaran. Pada awalnya
berpikir bahwa suplai oksigen ketergantungan patologis
hadir pada pasien dengan syok septik (yaitu, titik DO2
kritis meningkat dan VO2 tergantung pada DO2 pada
rentang yang lebih luas); Namun, ini
hubungan adalah unlikely.48-50
Pada syok, penurunan perfusi menyebabkan
metabolisme oksidatif terbatas mengakibatkan asidosis
laktat dari metabolisme anaerobik. Tingkat elevasi
laktat berkorelasi dengan kedua tingkat hipoperfusi dan
rate.51 kematian hipoperfusi Regional ditunjukkan
dengan penurunan lambung pH52,53 intramucosal dan
hati ve- desaturation.54 oksigen nous Namun, pada
kebanyakan pasien
Gambar 1 Hubungan antara konsumsi oksigen (VO2)
dan pengiriman oksigen (DO2).
dengan syok septik, ada juga tampaknya menjadi
ketidakmampuan jaringan untuk mengekstrak oksigen
dari blood.15 asidosis demikian laktat dapat terjadi
meskipun curah jantung normal dan saturasi oksigen
vena campuran (SvO2). Dalam cardio syok genic dan
hipovolemik, asidosis laktat terjadi hanya setelah
penurunan berat di SvO2.
DIAGNOSA
Langkah pertama untuk hasil yang sukses dengan
keadaan shock pengakuan awal. Hal ini penting untuk
diingat bahwa pasien diabetes, sirosis, neutropenia, dan
orang tua dapat mengembangkan syok septik tanpa
gambaran klinis yang khas atau sumber infeksi yang
jelas. evaluasi dasar harus mencakup panel metabolik,
hemogram, gas darah arteri, elektrokardiogram, dan xray dada. Penting untuk diingat bahwa penurunan kadar

hemoglobin terjadi di akhir syok hemoragik dan

kehilangan volume yang terbaik dinilai oleh
tanda-tanda hipoperfusi. Echocardiogram
NASIONAL bertambahnya ingly yang
digunakan dalam penilaian pasien shock; itu
adalah non-invasif, dapat dilakukan di samping
tempat tidur, dan dapat segera mengungkap atau
mengecualikan beberapa etiologi potensial dari
negara shock. Penelitian terbaru menunjukkan
bahwa tingkat procalcitonin merupakan
penanda yang baik dari infeksi dan dapat
membantu membedakan septic dari states.55,56
syok lainnya
Pemeriksaan fisik awal harus fokus pada tandatanda mengidentifikai hipoperfusi jaringan dan
pada differentiat- ing syok kardiogenik dari
jenis lain syok karena resusitasi volume awal
mungkin berbeda di bekas. Jika tanda-tanda
kelebihan cairan yang absen, kemungkinan
sumber kehilangan volume atau infeksi harus
agresif dicari akan. Tidak ada tanda-tanda,
gejala, atau uji laboratorium dengan sendirinya
merupakan diagnostik shock, mungkin dengan
pengecualian dari hipotensi yang mendalam.
Shock mudah untuk mendiagnosa ketika pasien
tiba di departemen darurat dengan beberapa
luka tusukan, perdarahan hebat, dan immeasurtekanan darah mampu. Masalahnya adalah
mengakui dalam presentasi lebih halus. Hal ini
diperlukan untuk mempertahankan indeks
kecurigaan yang tinggi dan waspada terhadap
sekelompok tanda spesifik dan gejala yang
dalam konteks klinis yang sesuai
memungkinkan diagnosis awal syok.
Tabel 3 hemodinamik Profil dan Main Terapi
Intervensi di Syok Serikat Berbagai
Profil hemodinamik Shock
Curah jantung
preload
afterload
kontraktilitas
Intervensi
Hipovolemik # # "N kristaloid atau koloid,
darah
kardiogenik
Septic # "" # inotropik, vasopresor
Cairan, vasopressors
Sebelum cairan
setelah cairan
Pulmonary Embolism # untuk N
"
##

N
##
# "#
#
N
terapi trombolitik
tamponade perikardial
Anafilaksis # # "N Pericardiocentesis
Cairan, inotropik, vasopresor
Sebelum cairan
setelah cairan
Adrenal untuk N
"#
N#
##
#
Cairan, steroid, inotropik, vasopresor
Sebelum cairan untuk N # # N Setelah cairan "N # N
Hipotensi hadir di sebagian besar negara shock dan
biasanya akan menarik perhatian dari dokter, tapi
sayangnya hanya terjadi sekali chanisms sayakompensasi kewalahan. Pada syok hipovolemik,
chycardia TA terjadi setelah 15% dari volume sirkulasi
hilang. Namun, meskipun tanda sensitif shock itu
spesifik, dan penting untuk menyadari bahwa respon
ini dapat tumpul pada pasien yang berada di blockers
b- atau calcium channel blockers. kulit berbintik-bintik
dan ekstremitas dingin, perubahan kesadaran, rasa
haus, air seni terkonsentrasi, oliguria, dan peningkatan
kreatinin dapat hadir. Dalam perdarahan hampir 30%
dari volume akan
hilang sebelum pasien menjadi hypotensive.57 An
sebelumnya
tanda penyempitan tekanan nadi karena catechoelevasi lamine-dirangsang tekanan darah diastolik
dalam menanggapi rendah beredar volume.57
Selanjutnya, tidak hanya bisa mengejutkan terjadi
tanpa adanya hipotensi, mungkin bertahan bahkan
sekali hipotensi memiliki telah terbalik. Tekanan darah
dapat dipertahankan dengan vasopressor pada biaya
memburuknya utang oksigen.
Pengukuran asam laktat adalah alat yang berguna untuk
menilai tingkat keparahan dan ikuti kecukupan euvers
mandat terapi, 58,59 tetapi perubahan asam laktat
mungkin tidak terjadi cukup awal untuk menjadi
penanda sentinel untuk shock. Setidaknya dalam sepsis,
kadar asam laktat yang tinggi telah terbukti terjadi
dengan oxygenation.60 intraseluler yang normal
Selanjutnya, kadar asam laktat yang tinggi dapat terjadi
karena kondisi komorbiditas, terutama kegagalan hati
karena dibersihkan oleh hati. Namun, dalam analisis
terbaru post hoc dari awal, yang diarahkan pada tujuan

terapi pada pasien sepsis dengan asidosis laktat

(> 4 mmol / L) dan tekanan arteri rata di atas
100 mm Hg, pasien dalam kelompok protokol
memiliki angka kematian secara signifikan
lebih rendah dibandingkan di group.61 terapi
standar
Pengukuran curah jantung dan SvO2, serta
perhitungan DO2, VO2, dan rasio ekstraksi
oksigen dapat dicapai dengan arteri pulmonalis
(PA) kateter. Meskipun kontroversi mengenai
penggunaannya, 62,63 yang
kateter secara luas digunakan, dan banyak efek
negatif yang dilaporkan pada hasil mungkin
hasil dari berdiri miskin pemahaman dan
pemanfaatan yang tidak tepat data.64 Selain
memastikan mengisi tekanan, aliran, dan
oksigen di- dadu, diagnosis patologis tertentu
terkait dengan syok dapat dilakukan (Tabel 3).
Peningkatan sisi kanan dan rendah PA tekanan
oklusi dalam pengaturan infark miokard rendah
akut harus meningkatkan kecurigaan dari
saturasi oksigen vena sentral ventrikel kanan
infarct.65 (ScvO2) lebih mudah untuk
mendapatkan dari arteri pulmonalis saturasi
vena campuran dan berpotensi menjadi gerbang
surro- baik untuk SvO2 di shock.66 septic
Hipoperfusi adalah ciri khas dari shock.
Menilaiment parameter transportasi oksigen adalah cara
terbaik untuk menentukan adanya hipoperfusi
jaringan global. Namun, hipoperfusi jaringan
regional dapat hadir meskipun nilai normal
variabel transportasi oksigen, defisit basa, dan
kadar asam laktat. tonometry lambung telah
terbukti untuk memprediksi kematian dan dapat
membantu menentukan perfusi splanknik dan
membimbing resuscitation.67,68 Akan tetapi,
kesulitan teknik dan interpretasi data, dan biaya
meningkat terkait dengan tonometry lambung,
telah membatasi penerapan klinis.
syok kardiogenik mungkin hadir dengan tandatanda peningkatan tekanan vena sentral, edema
paru, bunyi jantung ketiga, dan vasokonstriksi
perifer; meskipun edema paru dapat absen di
infark ventrikel kanan. Aritmia dan mitral
regurgitasi murmur juga dapat hadir.
Echocardiography membantu mengevaluasi
fungsi sistolik dan dapat mengungkapkan pecah
papiler otot, regurgitasi mitral, defek septum
ventrikel, dan bebas-dinding rupture.69
tanda Kussmaul, pulsus paradoksus, jantung
jauh terdengar pada auskultasi, dan penurunan

tegangan pada trocardiogram pemilu dapat hadir di

tamponade jantung. Pemerataan tekanan adalah
diagnostik dari kondisi ini dengan rata-rata kanan
atrium, ventrikel kanan akhir diastolik, dan tekanan
oklusi PA dalam 5 mm Hg dari satu
lain. Pusat tekanan tracing vena mungkin menunjukkan
'' x '' keturunan cepat dan '' y '' keturunan tumpul,
mencerminkan obstruksi aliran ventrikel.
Ekokardiogram mengungkapkan efusi perikardial, dan
dapat menunjukkan septum deviasi ventrikel runtuhnya
ventrikel kiri dan kanan selama sistol.
syok distributif, sering disebut sebagai '' hangat
shock, '' ditandai dengan vasodilatasi perifer dan status
jantung hiperdinamik yang berlaku sampai tahap-tahap
selanjutnya ketika depresi miokard akhirnya mengarah
ke penurunan curah jantung. Bukti infeksi, kehadiran
trauma tulang belakang atau pemicu untuk anafilaksis
akan membantu
membedakan etiologi yang mendasari. Krisis adrenal
mungkin hadir dengan nyeri perut, mual, muntah,
pothermia hidrokarbon, hipotensi refrakter,
hiponatremia, dan hiperkalemia.
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